Investigation on the virulence of non-encapsulated Streptococcus pneumoniae using liquid agar pneumonia model
Hideki Sakatani1, Masamitsu Kono1, Gen Sugita2
1Department of Otorhinolaryngology-Head and Neck Surgery, Wakayama Medical University, Kimiidera 811-1, Wakayama City, Wakayama, 641-8509, Japan.
Introduction:
Since the introduction of pneumococcal conjugate vaccine, there have been warnings of an increase in infections caused by non-vaccine type of Streptococcus pneumoniae strains. Among them, nonencapsulated Streptococcus pneumoniae (NESp) has been reported to cause invasive infections, especially in children and the elderly. Due to low virulence, however, basic experimental reports on invasive infections are limited.
Methods:
We applied a liquid-agar method to establish a mouse model of invasive NESp infection. Mice were intratracheally administered a bacterial suspension including agar. With this technique, we investigated the pathogenicity of NESp and the effect of Pneumococcal surface protein K (PspK), a specific surface protein antigen of NESp. NESp wild-type strain (MNZ11) and NESp pspK-deleted mutant strain (MNZ1131) were used in this study. The survival rate, number of bacteria, cytokine/chemokine levels in the bronchoalveolar lavage fluid, and histology of the lung tissue were evaluated.
Results:
Mice that were intratracheally administered MNZ11 developed lethal pneumonia with bacteremia within 48 h. Conversely, MNZ1131 showed predominantly low lethality without significant pro-inflammatory cytokine production. NESp was found to cause severe pneumonia and bacteremia upon reaching the lower respiratory tract, and PspK was a critical factor of NESp for developing invasive infections.
Conclusions:
The current study demonstrated the ability of NESp to develop invasive diseases, especially in connection with PspK by use of a mouse pneumonia model.
Insights
Non-encapsulated Streptococcus pneumoniae (NESp) can cause lethal pneumonia and bacteremia. Pneumococcal surface protein K (PspK) is crucial for NEsp
Area of Science:
- Microbiology
- Infectious Diseases
- Vaccinology
Background:
- Increased infections from non-vaccine type Streptococcus pneumoniae strains noted post-pneumococcal conjugate vaccine introduction.
- Non-encapsulated Streptococcus pneumoniae (NESp) strains are increasingly implicated in invasive infections, particularly in vulnerable populations.
- Limited experimental data exists on NEsp invasive infections due to perceived low virulence.
Purpose of the Study:
- To establish a mouse model for studying invasive non-encapsulated Streptococcus pneumoniae infections.
- To investigate the pathogenicity of NEsp and the role of Pneumococcal surface protein K (PspK) in invasive disease.
Main Methods:
- A novel liquid-agar intratracheal instillation method was employed to create a mouse model of invasive NEsp infection.
- Pathogenicity was assessed using wild-type NEsp (MNZ11) and a pspK-deleted mutant (MNZ1131).
- Evaluated outcomes included survival rates, bacterial load, cytokine/chemokine levels in bronchoalveolar lavage fluid, and lung histology.
Main Results:
- Intratracheal administration of wild-type NEsp (MNZ11) resulted in lethal pneumonia and bacteremia within 48 hours.
- The pspK-deleted mutant (MNZ1131) exhibited significantly lower lethality and minimal pro-inflammatory cytokine production.
- NESp causes severe pneumonia and bacteremia when it reaches the lower respiratory tract, with PspK identified as a critical virulence factor.
Conclusions:
- This study successfully demonstrated the capacity of NEsp to cause invasive disease using a developed mouse pneumonia model.
- Pneumococcal surface protein K (PspK) plays a critical role in the invasive potential of non-encapsulated Streptococcus pneumoniae.
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